Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/60460
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dc.contributor.authorRoss, D.en
dc.contributor.authorSchafranek, L.en
dc.contributor.authorHughes, T.en
dc.contributor.authorNicola, M.en
dc.contributor.authorBranford, S.en
dc.contributor.authorScore, J.en
dc.date.issued2009en
dc.identifier.citationCancer Genetics and Cytogenetics, 2009; 189(2):138-139en
dc.identifier.issn0165-4608en
dc.identifier.issn1873-4456en
dc.identifier.urihttp://hdl.handle.net/2440/60460-
dc.description.statementofresponsibilityDavid M. Ross, Lisa Schafranek, Timothy P. Hughes, Mario Nicola, Susan Branford, Joannah Scoreen
dc.language.isoenen
dc.publisherElsevier Science Incen
dc.rights© 2009 Elsevier Inc. All rights reserved.en
dc.subjectCell Line, Tumor; K562 Cells; Chromosomes, Human, Pair 9; Chromosomes, Human, Pair 22; Humans; Chromosome Breakage; Translocation, Genetic; Fusion Proteins, bcr-abl; Karyotyping; Gene Amplification; Base Sequence; Conserved Sequenceen
dc.titleGenomic translocation breakpoint sequences are conserved in BCR-ABL1 cell lines despite the presence of amplificationen
dc.typeJournal articleen
dc.identifier.rmid0020090276en
dc.identifier.doi10.1016/j.cancergencyto.2008.10.010en
dc.identifier.pubid39223-
pubs.library.collectionMedicine publicationsen
pubs.verification-statusVerifieden
pubs.publication-statusPublisheden
dc.identifier.orcidRoss, D. [0000-0001-7171-2935]en
dc.identifier.orcidHughes, T. [0000-0002-0910-3730]en
dc.identifier.orcidBranford, S. [0000-0002-1964-3626]en
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